Linked Life Data

19109150

Source:http://linkedlifedata.com/resource/pubmed/id/19109150

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-12-25
pubmed:abstractText
T cell-T cell Ag presentation is increasingly attracting attention. We previously showed that the in vitro OVA-pulsed dendritic cell (DC(OVA))-activated CD4(+) Th cells acquired OVA peptide/MHC (pMHC) class I and costimulatory molecules such as CD54 and CD80 from DC(OVA) and acted as CD4(+) Th-APC capable of stimulating OVA-specific CD8(+) CTL responses. In this study, we further applied the OVA-specific TCR-transgenic OT I and OT II mice with deficiency of various cytokines or costimulatory molecule genes useful for studying the molecular mechanisms underlying in Th-APC's stimulatory effect. We demonstrated that DC(OVA)-stimulated OT II CD4(+) Th-APC also acquired costimulatory molecules such as CD40, OX40L, and 4-1BBL and the functional pMHC II complexes by DC(OVA) activation. CD4(+) Th-APC with acquired pMHC II and I were capable of stimulating CD4(+) Th1 and central memory CD8(+)44(+)CD62L(high)IL-7R(+) T cell responses leading to antitumor immunity against OVA-expressing mouse B16 melanoma. Their stimulatory effect on CD8(+) CTL responses and antitumor immunity is mediated by IL-2 secretion, CD40L, and CD80 signaling and is specifically targeted to CD8(+) T cells in vivo via acquired pMHC I. In addition, CD4(+) Th-APC expressing OVA-specific TCR, FasL, and perforin were able to kill DC(OVA) and neighboring Th-APC expressing endogenous and acquired pMHC II. Taken together, we show that CD4(+) Th-APC can modulate immune responses by stimulating CD4(+) Th1 and central memory CD8(+) T cell responses and eliminating DC(OVA) and neighboring Th-APC. Therefore, our findings may have great impacts in not only the antitumor immunity, but also the regulatory T cell-dependent immune tolerance in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
182
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
193-206
pubmed:meshHeading
pubmed-meshheading:19109150-Amino Acid Sequence, pubmed-meshheading:19109150-Animals, pubmed-meshheading:19109150-Antigen-Presenting Cells, pubmed-meshheading:19109150-Antigens, CD44, pubmed-meshheading:19109150-CD8-Positive T-Lymphocytes, pubmed-meshheading:19109150-Cell Line, Tumor, pubmed-meshheading:19109150-Cytotoxicity Tests, Immunologic, pubmed-meshheading:19109150-Histocompatibility Antigens Class I, pubmed-meshheading:19109150-Histocompatibility Antigens Class II, pubmed-meshheading:19109150-Immunologic Memory, pubmed-meshheading:19109150-L-Selectin, pubmed-meshheading:19109150-Lymphocyte Activation, pubmed-meshheading:19109150-Melanoma, Experimental, pubmed-meshheading:19109150-Mice, pubmed-meshheading:19109150-Mice, Inbred C57BL, pubmed-meshheading:19109150-Mice, Knockout, pubmed-meshheading:19109150-Mice, Transgenic, pubmed-meshheading:19109150-Molecular Sequence Data, pubmed-meshheading:19109150-Peptide Fragments, pubmed-meshheading:19109150-Receptors, Interleukin-7, pubmed-meshheading:19109150-Th1 Cells
pubmed:year
2009
pubmed:articleTitle
CD4+ Th-APC with acquired peptide/MHC class I and II complexes stimulate type 1 helper CD4+ and central memory CD8+ T cell responses.
pubmed:affiliation
Research Unit, Research Division, Saskatchewan Cancer Agency and Department of Oncology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't